• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/25

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

25 Cards in this Set

  • Front
  • Back
very low RBC, Hgb, Hct
very high MVC
hemolyic anemia
peripheral smaer
polychromasia (mult-colored)
spherocytes (reticulocytes-new RBCs)
nucleated RBC
history clues
good nutrition
normal menses
recent illness
RBC smear
macrocytic (large cells) normochromic (normal color) anemia
marrow response to RBC loss
dramatic capacity to increase RBC production (by 6-10 times normal rate)
increase in reticulocytes-young, large RBC
mcv elevation
hemolytic anemia
mechanisms of anemia
decreased production
increased destruction
distinguish b/t w/ measurement of reticulocyte proportion
reticulocyte count
elevated-appropriate response (increased destruction/decreased survival)
low/normal-impaired/decreased production
hemolytic anemias
destruction of RBC faster than marrow can replace them
classified according to mechanism and location of RBC destruction
location of RBC destruction
intravascular-rapid destruction of RBC while in circlation (releases contents into circulation-toxic due to Hgb in plasma
extravascular-removal of RBC by reticuloendothelial system and macrophage disgestion (more common and less dangerous-slower destruction rate)
abnormalities of RBC cytoplasm (inherited)
enzyme defects
hemoglobinopathies
RBC membrane abnormalities
hereditary spherocytosis (inherited)
paroxysmal nocturnal hemoglobinuria (inherited)
spur cell anemia (acquired)
extrinsic factors (acquired)
hypersplenism
Ab: immune hemolysis
microangiopathic hemolysis
infections, toxins, mechanical
RBCs change to spherocytes due to loss of membrane
hereditary spherocytosis
autoimmun hemolytic anemia
clinical feature
hereditary-hyperbilirubinemia w/ possible jaundice
autoimmune-gradual fatigue
palor, splenomegaly
dark urine (tea colored)-from urine bilirubin
warm Ab
IgG (idiopathic or drug induced)
cold Ab
IgM-due to cold agglutinin disease or secondary infection
coombs test
detecting Abs to RBCs
direct-Ab bound to RBC surface
indirect-Ab circulating in serum that's reactive to RBC surface components
what accumulates in uncongugated form when large amounts of heme are released?
bilirubin
serumm scavenger of free hemoglobin-cleared by liver when bound
haptoglogin
purple hued young RBC, reflecting increase marrow prodcution
polychromatophilia
storage Fe sloughed into urine from Fe overloaded in renal tubule cell
hemosiderin
elevated MCV
round macrocytes (hemolysis)
oval macrocytes (vit. deficiency, MDS)
increased reticulocyte count
increased LDH
low haptoglobin
increased bilirubin
Coomb' direct-IgG positive
autoimmune hemolytic anemia
treatment
suppress immune system
1. steroids
2. splenectomy
3. monoclonal anti-lymphocyte Abs (anti-CD20)
4. chemotherapy